Open AccessPulmonary Inflammation and Injury in a Mouse Model of Non-Alcoholic Steatohepatitis
Author(s) -
Tanvi Banota,
Alexa Murray,
Laura E. Armstrong,
Bo Kong,
Grace L. Guo,
Andrew J. Gow,
Debra L. Laskin
Publication year - 2021
Publication title -
aresty rutgers undergraduate research journal
Language(s) - English
Resource type - Journals
ISSN - 2766-2918
DOI - 10.14713/arestyrurj.v1i3.177
Subject(s) - steatohepatitis , steatosis , fibrosis , inflammation , bronchoalveolar lavage , fatty liver , medicine , alcoholic hepatitis , lung , pathology , liver injury , alcoholic liver disease , cirrhosis , disease
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver condition that affects millions of individuals in the United States, of which approximately twenty percent of cases progress to non-alcoholic steato-hepatitis (NASH). NASH is characterized by macro-vascular steatosis and persistent inflammation in the liver, which can lead to fibrosis. Evidence suggests potential effects of NAFLD and NASH on the devel-opment of pulmonary pathologies, but the interaction between the liver and the lung is not well under-stood. In this study, we assessed the impact of NASH development on lung inflammation and fibrosis over time. Male C57BL/6J mice were fed control (10% kCal) or high-fat (HFD) (60% kCal) diets. Liver tissue, lung tissue, and bronchoalveolar lavage (BAL) fluid were collected after 1, 3, and 6 months of feeding. Histopathologic evaluation of livers from HFD-fed mice at 6 months confirmed the development of NASH. In the lung, we observed histopathologic al-terations, including inflammatory cell infiltration, li-pid-laden macrophages, septal damage, and epi-thelial thickening at 6 months. Gene expression anal-ysis of whole lung tissue revealed changes in genes related to inflammation (IL-1B), fibrosis (CTGF), and lipid metabolism (ApoA1). These results characterize an association of pulmonary complications during simple steatosis to NASH transition, suggesting lung-liver crosstalk.